Focal adhesion kinase signaling in cardiac hypertrophy and failure

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Author(s):	K.G. Franchini ^[1] ; C.F.M.Z. Clemente ^[2] ; T.M. Marin ^[3] Total Authors: 3
Affiliation:	^[1] Universidade Estadual de Campinas. Faculdade de Ciências Médicas. Departamento de Clínica Médica - Brasil ^[2] Universidade Estadual de Campinas. Faculdade de Ciências Médicas. Departamento de Clínica Médica - Brasil ^[3] Universidade Estadual de Campinas. Faculdade de Ciências Médicas. Departamento de Clínica Médica - Brasil Total Affiliations: 3
Document type:	Journal article
Source:	Brazilian Journal of Medical and Biological Research; v. 42, n. 1, p. 44-52, 2009-01-00.
Abstract
Focal adhesion kinase (FAK) is a broadly expressed tyrosine kinase implicated in cellular functions such as migration, growth and survival. Emerging data support a role for FAK in cardiac development, reactive hypertrophy and failure. Data reviewed here indicate that FAK plays a critical role at the cellular level in the responses of cardiomyocytes and cardiac fibroblasts to biomechanical stress and to hypertrophic agonists such as angiotensin II and endothelin. The signaling mechanisms regulated by FAK are discussed to provide insight into its role in the pathophysiology of cardiac hypertrophy and failure. (AU)

FAPESP's process:	06/54878-3 - Pathogenesis of cardiac hypertrophy and failure: mechanisms activated by mechanical stress
Grantee:	Kleber Gomes Franchini
Support Opportunities:	Research Projects - Thematic Grants